Pathogenicity of Toxoplasma gondii through B-2 Cell-Mediated Downregulation of Host Defense Responses

IFN‐γ is the primary mediator of anti‐parasite effector mechanisms against Toxoplasma gondii. After intraperitoneal infection with the Fukaya strain of T. gondii, unirradiated IFN‐γ knock‐out (GKO) mice transferred with wild type (WT) CD8+ effector T cells from infected mice failed to induce the production of IFN‐γ and died, whereas irradiated (IR) GKO mice transferred with WT CD8+ T cells induced IFN‐γ production and survived more than 6 months. IR GKO mice transferred with WT CD8+ T cells together with GKO B‐2 cells died 8 days after infection, whereas those transferred with WT CD8+ T cells together with B‐1a or T cells survived. B‐2 cells of infected GKO mice activated CD11b+ cells for IL‐4 production, and down‐regulated NO release, STAT1 phosphorylation, and interferon regulatory factor‐1 expression in the peritoneal exudates cells of IR GKO mice transferred with WT CD8+ T cells together with GKO B‐2 cells after infection. Thus, B‐2 cells in T. gondii‐infected mice act as suppressor cells in the host defense of infected mice.